Supraventricular arrhythmias (SVAs) are characterized by abnormal rhythms that arise in the atria or the atrioventricular node (AV node), essentially arising in any tissue located anatomically above the ventricles. An SVA can exhibit heart rates between approximately 140 beats per minute (bpm) and approximately 250 bpm. The most common SVAs are atrial flutter and atrial fibrillation. Many SVAs involve the AV node, for example, AV nodal reentry tachycardia (AVNRT) where the arrhythmia repeatedly re-excites tissue via reentrant pathway through the AV node.
Atrial flutter can result when an early beat triggers a “circus circular current” that travels in regular cycles around the atrium, pushing the atrial rate up to approximately 250 bpm to approximately 350 bpm. The atrioventricular node between the atria and ventricles will often block one of every two beats, keeping the ventricular rate at about 125 bpm to about 175 bpm. This is the pulse rate that will be felt, even though the atria are beating more rapidly. At this pace, the ventricles will usually continue to pump blood relatively effectively for many hours or even days. A patient with underlying heart disease, however, may experience chest pain, faintness, or even heart failure as a result of the continuing increased stress on the heart muscle. In some individuals, the ventricular rate may also be slower if there is increased block of impulses in the AV node, or faster if there is little or no block.
If the cardiac impulse fails to follow a regular circuit and divides along multiple pathways, a chaos of uncoordinated beats results, producing atrial fibrillation. Fibrillation commonly occurs in conjunction with atrial enlargement associated with heart disease. Fibrillation can however, also occur in the absence of any apparent heart disease. In fibrillation, the atrial rate can increase to more than 350 bpm and cause the atria to fail to pump blood effectively. Under such circumstances, the ventricular beat may also become haphazard, producing a rapid irregular pulse. Although atrial fibrillation may cause the heart to lose approximately 20 to 30 percent of its pumping effectiveness, the volume of blood pumped by the ventricles usually remains within the margin of safety, again because the atrioventricular node blocks out many of the chaotic beats. Hence, during atrial fibrillation, the ventricles may contract at a lesser rate than the atria, for example, of approximately 125 bpm to approximately 175 bpm.
Various studies have reported on interactions between the autonomic nervous system and SVAs. For example, Schlepper, “Effects of the autonomic nervous system in supraventricular arrhythmia”, Z. Kardiol., 75, Suppl. 5: 35–40 (1986), original text in German, reported that “influences of the autonomic nervous system may cause modifications of the initiation, continuation and discontinuation of supraventricular rhythm disturbances”. In particular, Schlepper reported that “in atrial fibrillation and atrial flutter the influence of the autonomic nervous system is apparent in a form of the vagotonically and sympathotonically evoked paroxysms”. Indeed, a study by Ringdahl, “Vagally mediated atrial fibrillation in a young man,” Arch. Fam. Med., 9:389–390 (2000), recognized that atrial fibrillation may be parasympathetically or sympathetically mediated. Ringdahl reported that sympathetic effects are common in middle-aged and elderly patients with underlying heart disease while, in the young, where heart disease is typically not present, vagal influences are more likely to predominate. Hence, for patients diagnosed with heart disease, increased sympathetic tone is a likely factor in arrhythmia initiation.
While the Ringdahl study indicates that both autonomic branches can play a role in initiating arrhythmia (the responsible branch determined largely by patient age and disease state), both branches may also play a role in terminating arrhythmia. Perhaps the simplest approach to termination of an SVA through parasympathetic stimulation involves Valsalva's maneuver. Valsalva's maneuver involves having a patient (i) inhale and hold her breath, (ii) bear down while holding her breath, as if to have a bowel movement, and (iii) hold the position for approximately 20 seconds to approximately 30 seconds. This maneuver aims to terminate a SVA by increasing parasympathetic tone and consequently slow conduction through the AV node. Another technique involves application of pressure to the carotid sinuses. For example, a physician may apply gentle and steady pressure over a patient's right carotid sinus and hold for approximately 5 to approximately 10 seconds. If a favorable response does not results from application of pressure to the right carotid sinus, then after a short wait (e.g., approximately 2 to 4 minutes), the technique may be applied to the left carotid sinus.
In general, studies show that parasympathetic stimulation can terminate SVAs. However, SVA termination therapies that rely on parasympathetic stimulation have not been implemented using implantable delivery technology. Therefore, a need exists for methods and/or devices that can stimulate parasympathetic pathways to treat SVAs. In particular, a need exists for termination of sympathetically mediated SVAs via parasympathetic stimulation.